Determinants of maximal oxygen uptake in severe acute hypoxia

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Abstract
To unravel the mechanisms by which maximal oxygen uptake (V˙o 2 max) is reduced with severe acute hypoxia in humans, nine Danish lowlanders performed incremental cycle ergometer exercise to exhaustion, while breathing room air (normoxia) or 10.5% O2 in N2(hypoxia, ∼5,300 m above sea level). With hypoxia, exercise PaO2 dropped to 31–34 mmHg and arterial O2 content (CaO2) was reduced by 35% ( P < 0.001). Forty-one percent of the reduction in CaO2 was explained by the lower inspired O2 pressure (Pi O2) in hypoxia, whereas the rest was due to the impairment of the pulmonary gas exchange, as reflected by the higher alveolar-arterial O2 difference in hypoxia ( P < 0.05). Hypoxia caused a 47% decrease inV˙o 2 max (a greater fall than accountable by reduced CaO2). Peak cardiac output decreased by 17% ( P < 0.01), due to equal reductions in both peak heart rate and stroke volume ( P < 0.05). Peak leg blood flow was also lower (by 22%, P < 0.01). Consequently, systemic and leg O2 delivery were reduced by 43 and 47%, respectively, with hypoxia ( P < 0.001) correlating closely with V˙o 2 max( r = 0.98, P < 0.001). Therefore, three main mechanisms account for the reduction ofV˙o 2 max in severe acute hypoxia: 1 ) reduction of Pi O2, 2 ) impairment of pulmonary gas exchange, and 3 ) reduction of maximal cardiac output and peak leg blood flow, each explaining about one-third of the loss inV˙o 2 max.